The Ignorant

Today's case is awesome - please read all the way to the end ... we need your advice!

Gregor had been operated 12 years ago for a aortic valve stenosis, mitral regurgitation, and coronary artery disease. He received two bioprosthetic valves and a bypass. The operation went off well, but problems arose later: postoperative bleeding, atrial fibrillation, wound infection. Gregor was in the intensive care unit for more than 3 weeks. However, he was strong and the anesthetists did a great job – Gregor recovered and continued to lead a happy life.

His kidneys had suffered, but his renal dysfunction improved gradually. Six years after surgery Gregor noticed mild shortness of breath. Still, he did not wish to see a doctor. He did not consider the fact that the problems with his heart might be recurring. Who could blame him after what he had gone through?

Two years ago, after an episode of dyspnea, he was dragged to our clinic. Something was, indeed, wrong with his valve. We suggested reoperation, but Gregor stuck his head in sand. “I would rather jump from an airplane without a parachute,” he said. When he was in the midst of pulmonary edema and gained 8 kg with peripheral edema, he did knock at the door of the doctor’s office again. This time he came with an ambulance. The immediate diagnosis was severe pulmonary hypertension.

Here is what we found on the echo:

 Parasternal long-axis view

Does the bioprosthetic valve look normal? What about the size of the right ventricle? Is septal motion normal?


A huge right ventricle and a right atrium with abnormal septal motion.


CW Doppler of tricuspid regurgitation; the maximal velocity is
3.8 m/sec

This truly is pulmonary hypertension: pulmonary pressure was estimated at 73 mmHg. What is the cause of pulmonary hypertension? To answer the question we have to look at the following spectrum:

CW Doppler of mitral inflow across the bioprosthesis

Is this the pattern of a “normal” mitral bioprosthesis? Certainly not. The mean gradient was 22 mmHg (very high) and the pressure half-time was 295ms. However there is more:

Placing the transducer to the left, towards the lung (right image), and then
towards  the abdomen (left image) yielded these pictures.

We have pleural effusion and ascites - findings that explain his symptoms.Both are typical signs of right heart failure. So the next thing to do is to look at right ventricular function:

M-mode of the tricuspid annular plane (TAPSE) on the right and the TDI
spectrum of the basal  free right ventricular lateral wall.

Yes, his right ventricular function is very poor. TAPSE is only 8 mm (it should be 15-17 mm) and TDI velocity in the free basal RV wall very low at 3 cm/s (normally >15 to 17 mm).
Putting it all together
Can you come up with the correct diagnosis? What happened? Gregor has severe obstruction of the bioprosthesis. Renal dysfunction might have been the trigger, causing degeneration of the valve. The hemodynamics here is very similar to mitral stenosis, which also leads to post-capillary pulmonary hypertension, tricuspid regurgitation, and eventually right heart failure.
What now?
Obviously, the only solution to the problem was reoperation and Gregor was begging for it. He really was suffering. There is only one problem. Reduced right ventricular function is one of the most important predictors of survival for cardiac surgery. And his function is very very poor. Should we still go ahead? Or is there another option? Let us know what your approach would be in the Comments section. I promise I will tell you what we did in the next post.
What is the key message here?
Some things need to be resolved quickly and Gregor was not wise to stick his head in sand. Pulmonary hypertension is evil and eventually leads to right heart failure. Looking for pulmonary hypertension is therefore one of the most important aspects of echocardiography and should never be omitted, especially in patients with left heart disease.

yours truly Tommy Binder & the 123sonography team